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酵母热休克蛋白70同源物Ssa是翻译所必需的,并且在翻译核糖体上与Sis1和Pab1相互作用。

The yeast hsp70 homologue Ssa is required for translation and interacts with Sis1 and Pab1 on translating ribosomes.

作者信息

Horton L E, James P, Craig E A, Hensold J O

机构信息

Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.

出版信息

J Biol Chem. 2001 Apr 27;276(17):14426-33. doi: 10.1074/jbc.M100266200. Epub 2001 Jan 22.

Abstract

The 70-kDa heat shock proteins are molecular chaperones that participate in a variety of cellular functions. This chaperone function is stimulated by interaction with hsp40 proteins. The Saccharomyces cerevisiae gene encoding the essential hsp40 homologue, SIS1, appears to function in translation initiation. Mutations in ribosomal protein L39 (rpl39) complement loss-of-function mutations in SIS1 as well as PAB1 (poly(A)-binding protein), suggesting a functional interaction between these proteins. However, while a direct interaction between Sis1 and Pab1 is not detectable, both of these proteins physically interact with the essential Ssa (and not Ssb) family of hsp70 proteins. This interaction is mediated by the variable C-terminal domain of Ssa. Subcellular fractionations demonstrate that the binding of Ssa to ribosomes is dependent upon its C terminus and that its interaction with Sis1 and Pab1 occurs preferentially on translating ribosomes. Consistent with a function in translation, depletion of Ssa protein produces a general translational defect that appears similar to loss of Sis1 and Pab1 function. This translational effect of Ssa appears mediated, at least in part, by its affect on the interaction of Pab1 with the translation initiation factor, eIF4G, which is dramatically reduced in the absence of functional Ssa protein.

摘要

70 kDa热休克蛋白是参与多种细胞功能的分子伴侣。这种伴侣功能通过与hsp40蛋白相互作用而被激活。酿酒酵母中编码必需hsp40同源物SIS1的基因似乎在翻译起始中发挥作用。核糖体蛋白L39(rpl39)的突变可弥补SIS1以及PAB1(聚腺苷酸结合蛋白)功能丧失的突变,这表明这些蛋白之间存在功能相互作用。然而,虽然无法检测到Sis1与Pab1之间的直接相互作用,但这两种蛋白都与hsp70蛋白的必需Ssa(而非Ssb)家族发生物理相互作用。这种相互作用由Ssa的可变C末端结构域介导。亚细胞分级分离表明,Ssa与核糖体的结合依赖于其C末端,并且它与Sis1和Pab1的相互作用优先发生在正在翻译的核糖体上。与在翻译中的功能一致,Ssa蛋白的缺失会导致普遍的翻译缺陷,这与Sis1和Pab1功能丧失时出现的情况相似。Ssa的这种翻译效应似乎至少部分是由其对Pab1与翻译起始因子eIF4G相互作用的影响介导的,在缺乏功能性Ssa蛋白时,这种相互作用会显著降低。

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